Peripheral Nervous System Flashcards
Types of axonal injury in PNS
Wallerian degeneration
Axonal degeneration
Segmental demyelination
Wallerian degeneration
Transaction of axons (by trauma or compression) —> loss of distal segment, axon/myelin at injury site, proximal segment of injury next to node —> axonal flow halted —> accumulation of neuro filaments, mitochondria, debris —> swelling of degenerated axon (spheroid) —> distal segment Wallerian degeneration (removed by macrophages) —> axonal sprouting/segmental remyelination—> NMJ reestab.
Central chromatolysis also observed, but reversible
Factors affecting success of Wallerian degeneration
Endometrium must be intact
How distal is the lesion? How far apart are the severed ends of nerve? How much damage/debris sis around injury site
Neuroma
Result of unsuccessful PNS regeneration
Small painful nodule of axons/Schwann cells
Dysfunction of healing (not neoplasm)
Axonal degeneration
Occurs due to metabolic derangement of neuron —> death of distal portion of axon (lose both myelin and axon)
Can look similar to Wallerian, but different cause (inherited, metabolic, toxic, and diseases)
Regeneration poor
Polyneuritis equi
(Aka Cauda Equina syndrome)
Progressive inflammation of caudal spinal cord / nerve trunk so of cauda equine of horses - unknown cause (immune mediated?)
Clincial signs: ataxia, pain, dropped tail, urinary incontinece, fecal retention, muscle loss
Nerve roots thickened, fusiform, yellow discoloration; granulomatous inflammation/fibrosis
Histology of polyneuritis
Nodular aggregates of granulomatous inflammation around nerves
Characterized by macrophages
Expansion of perineurium/epineurium by fibrosis
Acquired myasthenia gravis
Auto-antibodies to acetyl choline receptor block function
Responds to anti-acetylcholinesterase therapy
Can be self-limiting
Congenital myasthenia gravis
Deficiency of acetyl choline receptors (no circulating antibodies to ACh receptors)
Responsive to anti-cholinesterase therapy - reduced cholinesterase —> increased available ACh at synapse
Jack Russel terriers, springer spaniels, smooth haired fox terriers
Infectious causes of NMJ disorders
Botulism
Tetanus
Botulism
Botulinum toxin from C. Botulinum blocks release of acetylcholine
Generalized FLACCID paralysis
Tetanus
Tetanospasmin toxin from C. Tetani —> binds inhibitory interneurons —> blocks release of inhibitory neurotransmitter
SPASTIC/rigid paralysis
Equine laryngeal hemiplegia
Progressive (Wallerian) degeneration of axons of left recurrent laryngeal nerve
Denervation atrophy of cricoarytenoideus dorsalis muscle of left side of larynx
Causes: trauma to nerves, extension of inflammation from guttural pouch
Brachial plexus avulsion
Acute exacerbated abduction of forelimb/stretching of brachial plexus nerves
Causes: jumping from high place
Recovery depends on severity of stretching/fibrosis
Equine peripheral neuropathy
Uncommon
Injury to nerve/nerve roots of brachial plexus (trauma, poorly fitted harness collar)